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Lower risk of cerebral palsy in the child if the parents have higher educationhttps://ije-blog.com/2018/06/29/lower-risk-of-cerebral-palsy-in-the-child-if-the-parents-have-higher-education/
https://ije-blog.com/2018/06/29/lower-risk-of-cerebral-palsy-in-the-child-if-the-parents-have-higher-education/#respondFri, 29 Jun 2018 00:00:25 +0000http://ije-blog.com/?p=2059Continue reading Lower risk of cerebral palsy in the child if the parents have higher education]]>Ingeborg Forthun

Cerebral palsy is the most common physical disability among children, with about two per 1000 live-born infants being diagnosed with the disorder. In most children with cerebral palsy, the disability is caused by damage to the immature brain during pregnancy or birth that results in problems with movement.

Denmark and Norway have low income inequality and free access to education and offer high-quality antenatal care to pregnant women free of charge. Nevertheless, in our study recently published in the International Journal of Epidemiology, we found that the risk of having a child with cerebral palsy in these two countries varies by the parents’ educational level, and this educational gradient has been surprisingly stable over time.

In our study, we aimed to assess whether the risk of having a child with cerebral palsy varied by different measures of parental socioeconomic status in Denmark and Norway. We found a strong educational gradient in the risk of having a child with cerebral palsy in both countries – the higher the education of the parents, the lower the risk. There was a one-third reduction in risk among those with a Bachelor or higher degree compared with parents with only primary or lower secondary education. Decreased risks of the same magnitude were found independently for both mothers and fathers, and these trends were stable over the past four decades, despite a large increase in the proportion of parents with higher education, especially among women.

The Nordic countries are known for their redistributive tax system and social policies aimed at reducing socioeconomic differences. The Nordic model has been successful in many respects – for example, Denmark and Norway rank as two of the OECD countries with the lowest income inequality. However, paradoxically, the social inequality in adverse health outcomes is larger than in many other European countries, and increasing.

In our study, we found no association between household income and the risk of having a child with cerebral palsy, when adjusting for parental education and age. Among parents-to-be in the Nordic setting, income may be a poorer marker of socioeconomic status – income has been more responsive to social policy, and parents are early in their careers when they have children. In addition, a higher income does not necessarily result in healthier behaviour.

A recent study reported a decreasing prevalence of cerebral palsy in Norway since 1999. The same has been found in a multicenter study in Europe. This positive trend is believed to be due to improvements in obstetric and neonatal care. Still, in a majority of children with cerebral palsy, the cause is unknown. It may be due to either genetic or environmental factors in pregnancy that cause damage to the brain before birth or increase the infant’s susceptibility to brain damage during or shortly after birth. It is important to continue research to identify causal factors for cerebral palsy in these children.

Our study suggests that risk factors that differ by socioeconomic status – such as maternal overweight, smoking, poor diet, maternal infections, paracetamol use and chronic disease – may play a role, and that there could be room for further prevention. Maternal overweight, smoking, genitourinary infections and paracetamol use have been linked to increased risk of cerebral palsy, while chronic disease and dietary factors have been less often investigated.

We also hypothesise that recurrence of cerebral palsy within families could partly explain our results: if cerebral palsy in parents affects their chance of undertaking higher education and increases the risk of having a child with cerebral palsy. We were not able to assess these potential underlying mechanisms in our study, but we hope to answer some of these questions in ongoing studies.

The Obstetrics and Periodontal Therapy (OPT) Study was an NIH-funded randomised controlled trial designed to evaluate whether periodontal treatment in pregnant women had any effect on preterm birth; its findings were published in 2006. The investigators randomly assigned about 800 women who had been pregnant for less than 16 weeks, and had periodontal disease, to one of two groups. One group received periodontal treatment during pregnancy, whereas the other group received treatment after pregnancy.

Although the study found that treatment controlled periodontal infection and reduced the microorganism load, there was no difference in preterm birth rates between the two groups. The investigators concluded that treating periodontal disease during pregnancy did not affect the risk of preterm birth. However, they also found that there were more stillbirths in the group that received treatment after pregnancy, suggesting that periodontal treatment may improve survival of fetuses. The potential bias resulting from the intervention affecting both the outcome (in this case, preterm birth) and survival (in this case, stillbirth) was acknowledged as a limitation.

Since then, newer epidemiological methods have been developed to quantify the bias that can occur in a randomised controlled trial when the intervention affects both the outcome and survival. As the OPT investigators had made data from their study available in the public domain, we were able to reanalyse their data, applying these newly developed methods, in our study published recently in the International Journal of Epidemiology.

To apply these new methods, the study question is conceptualised as a hypothetical. In this case, suppose we compared preterm birth risk among women who had live births in both treatment groups in the OPT study if – hypothetically – both groups received treatment during pregnancy (contrary to what actually happened) (Figure 1). The difference in preterm birth risk between the two groups in the hypothetical comparison would then be the degree of bias that was caused by stillbirths, which could be used to correct for bias in the clinical trial estimates. Because these methods test the hypothetical, they are called ‘counterfactual’ or ‘potential outcomes’ methods.

Figure 1. (A, left) What actually happens in an RCT when treatment benefits fetal survival. (B, right) Mothers who have live births in the RCT. If, hypothetically, all these mothers receive periodontal treatment, more preterm births would be expected in the treatment group because it has more high-risk mothers. The difference in preterm birth risk between the treatment and control groups is the excess risk caused by pregnancy losses in an RCT when treatment benefits fetal survival. (Credit: Bryn Davis)

In our study, we reanalysed the OPT data using counterfactual methods and found that if women with periodontal disease were treated for the disease before 20 weeks of pregnancy, they may have a lower risk of preterm birth.

Periodontal infection is controlled by treatment that is safe and well-tolerated. However, many people with early periodontal disease may not know that they have it (Figure 2). Our findings suggest that encouraging women to visit a dentist, either when they are planning to get pregnant or in their fifth or sixth month of pregnancy, may help prevent adverse birth outcomes.

Childhood overweight and obesity are a global public health problem. In high-income countries, obesity follows socioeconomic patterns, in that people with a lower socioeconomic position are more likely to be overweight or obese than those with a higher socioeconomic position. Poor diet is a key risk factor for excess weight gain. It is also a risk factor that we can do something about.

In our study recently published in the International Journal of Epidemiology, we examined the contribution of unhealthy food and drink consumption to the development of socioeconomic inequalities in weight among children in Australia. We found that socioeconomic differences in unhealthy food and drink intake emerge from the first year of life and persist throughout childhood. Almost one in two children with a low socioeconomic position were consuming sweet drinks in their first year of life, compared with one in four children with a higher socioeconomic position.

We also found that the inequalities in the consumption of unhealthy food and drinks throughout childhood contributed to the development of inequalities in excess weight at the age of 10–11 years. This is the first study to demonstrate the effect of cumulative consumption of unhealthy food and drinks from birth and throughout childhood on socioeconomic differences in children’s weight.

Unhealthy (or ‘discretionary’) food and drinks are typically those with excess fat, sugar and salt, such as processed meats, pies and savoury pastries, commercially fried foods, potato crisps, confectionery and chocolate, sweet biscuits and cakes, and sugar-sweetened beverages. These items contribute up to 40% of Australian children’s total dietary intake.

Frequent consumption of unhealthy food and drinks in childhood is concerning, as it is during early childhood that taste preferences and dietary habits are established. Furthermore, obese children are likely to become obese adults, and the consequences, including adverse physical and psychological effects, are also likely to persist into adulthood. Greater consumption of unhealthy food and drinks in early life among children from lower socioeconomic backgrounds, accompanied by higher rates of overweight and obesity, means these children are set to carry a disproportionate burden of poor diet and excess weight from a very young age.

Parents of young children face an increasingly complex world when it comes to choosing food and drinks for their children. The ever-increasing availability of unhealthy options, prolific marketing, confusing product labels and misleading health claims create an environment that promotes unhealthy food and drink choices. We must change the environment to make the healthy choice the easy choice for parents and their children.

Recommendations from the WHO Commission on Ending Childhood Obesity call for coordinated government action to promote intake of healthy food and reduce consumption of unhealthy food and sweet drinks among children. This starts with providing nutritional advice to women throughout the antenatal period and supporting parents to introduce and offer a wide variety of foods to infants and young children.

It is clear that there is no single solution to the problem of childhood obesity. Improving children’s diets must be part of a comprehensive, government-led strategy that tackles obesity risk factors from the prenatal period throughout childhood and beyond. This strategy must include an equity focus, to ensure that those with the greatest social and economic disadvantage are not left behind.

Alexandra Chung is a PhD candidate at the School of Public Health and Preventive Medicine, Monash University, and visiting researcher at the Global Obesity Centre (GLOBE), World Health Organization Collaborating Centre for Obesity Prevention, School of Health & Social Development, Deakin University.

]]>https://ije-blog.com/2018/03/06/junk-food-in-childhood-contributes-to-socioeconomic-inequalities-in-overweight-and-obesity/feed/0ijeeditorialAlexandra_Chung_imagesmoothies-1646627_128000P1400000ncSRcEAMCan we promote physical activity at the population level?https://ije-blog.com/2018/02/19/can-we-promote-physical-activity-at-the-population-level/
https://ije-blog.com/2018/02/19/can-we-promote-physical-activity-at-the-population-level/#respondMon, 19 Feb 2018 03:01:42 +0000http://ije-blog.com/?p=2037Continue reading Can we promote physical activity at the population level?]]>Findings from a community-based 5-year cluster randomised trial

Masamitsu Kamada, I-Min Lee and Ichiro Kawachi

Despite the well-known health benefits of physical activity, physical inactivity remains highly prevalent globally. Effective population strategies to promote physical activity are needed to reduce the global burden of non-communicable diseases stemming from physical inactivity. But the question is: how do we effectively promote physical activity at the population level, such as in entire communities?

Physical activity is shaped by diverse influences at the individual, environmental, societal and policy levels. As such, multilevel and intersectoral approaches are needed to achieve population-wide changes in physical activity.

Evidence from a few short-term trials has highlighted the difficulty of achieving population-level improvements in physical activity through multi-strategic community-wide interventions. In contrast to individual-level interventions, large-scale social interventions face challenges associated with their complex nature and real-world environments that are difficult to control, and it may take considerably longer to influence population levels of physical activity.

Our study, recently published in the IJE, examined the effectiveness of a 5-year community-wide intervention for promoting physical activity in middle-aged and older adults using a cluster randomised design. The study was conducted in Unnan City, Shimane, Japan.

In this first such cluster randomised trial of a long community-wide intervention for population-level physical activity, adults achieving recommended levels of physical activities increased in the intervention communities compared with the control community (4.6 percentage points of change difference).

The intervention was effective for promoting all types of recommended physical activities — aerobic, flexibility and muscle-strengthening activities. However, a bundled approach, which attempted to promote all forms of recommended physical activities simultaneously, was not effective.

Intervention emphases in each phase and logic model of the study

Going back to the question, is it possible to promote physical activity at the population level? Based on our study, the answer is yes. The multi-strategic community-wide intervention was effective in promoting physical activity. More importantly, how we promoted physical activity was a critical determining factor of success. For example, the failure of our bundled (all-in-one) approach suggests that “one thing at a time” — a basic principle of social marketing — may be key to the successful dissemination of physical activity recommendations.

As the World Health Organization and other health agencies recommend multiple types of physical activity (aerobic and muscle-strengthening activities, etc) as a key lifestyle factor for preventing non-communicable diseases, a phased strategy (eg, aerobic activity in the first phase, and muscle-strengthening activity later) is worth considering, especially when resources are limited.

In addition, based on the existing literature, including our current and previous investigations (1-year and 3-year evaluations), one year may be too short to achieve population-wide changes in physical activity through community-wide interventions. Focused promotion strategies sustained for several years may be necessary.

Public health professionals also need to be reminded that dissemination of knowledge does not always translate to dissemination of behaviour change. To effectively change behaviour at the population level, we need to carefully design our interventions.

In our study, the intervention adopted social marketing techniques. These techniques apply marketing principles to create, communicate and deliver value that influences target audience behaviour that benefits society as well as the target audience. We deployed all six social marketing benchmark criteria — behavioural objective, audience segmentation, audience research, exchange, marketing mix and competition — which is rare in physical activity interventions in older populations. Sophisticated social marketing processes should sharpen intervention strategies to achieve actual behaviour change (not just knowledge improvement) at the population level.

An example of a poster based on social marketing techniques [“If such a short distance is fine, I’m a regular walker, too.” Everybody walks for a short distance. Walk for 10 minutes for good function of lower back and knees ♪]Though not always practical or feasible, the design of our study (cluster randomised trial) is considered the optimal design to develop practice-based evidence. The original one-year result from this project received the highest quality ranking (ie, lowest risk of bias) in a review article of 33 studies examining the effectiveness of community-wide interventions. Further high-quality studies and systematic reviews could yield deeper insights into effective population approaches to promote physical activity.

Masamitsu Kamada is a research fellow at the Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, and the Sasakawa Sports Foundation Overseas Research Fellow. His research focuses on physical activity epidemiology and population health interventions.

I-Min Lee is an associate epidemiologist at the Division of Preventive Medicine, Brigham and Women’s Hospital, and a professor at the Harvard Medical School and the Harvard T.H. Chan School of Public Health.

Ichiro Kawachi is the John L. Loeb and Frances Lehman Loeb Professor of Social Epidemiology and Chair of the Department of Social and Behavioral Sciences at the Harvard T.H. Chan School of Public Health.

]]>https://ije-blog.com/2018/02/19/can-we-promote-physical-activity-at-the-population-level/feed/0ijeeditorialKamada authorsFig.LogicModel121011_うんなんポスター２種What has contributed to the reduction in mortality rate for children aged under 5 in sub-Saharan Africa?https://ije-blog.com/2018/02/12/what-has-contributed-to-the-reduction-in-mortality-rate-for-children-aged-under-5-in-sub-saharan-africa/
https://ije-blog.com/2018/02/12/what-has-contributed-to-the-reduction-in-mortality-rate-for-children-aged-under-5-in-sub-saharan-africa/#respondMon, 12 Feb 2018 04:36:33 +0000http://ije-blog.com/?p=2029Continue reading What has contributed to the reduction in mortality rate for children aged under 5 in sub-Saharan Africa?]]>Yoko Akachi, Maria Steenland and Günther Fink

Reducing child mortality remains one of the key objectives of the Sustainable Development Goals. Remarkable progress has been made over the past 25 years, with the global number of deaths of children aged under 5 falling from 13 million in 1990 to six million in 2015. Yet little is known about the relative contributions of specific public health interventions and general improvements in socioeconomic status and educational attainment over the same period.

To better understand the contributions of these factors, in our study published recently in the IJE we made a major effort to convert 78 Demographic and Health Surveys into a longitudinal dataset that allowed us to track all key variables at a country regional (typically provincial) level in sub-Saharan Africa over time. The final dataset covered 562,896 child observations across 241 regions in 24 countries for the period 1990–2014 (Figure 1).

Figure 1. Spatial coverage of dataset

We considered an extensive list of factors contributing to declines in child mortality. The primary public health interventions included were:

bed net coverage for malaria prevention

water and sanitation infrastructure

vaccination coverage

institutional deliveries

modern contraceptive usage

antenatal care

neonatal tetanus protection

low body mass index

intermittent preventive treatment for malaria during pregnancy

caesarean section rate

oral rehydration therapy, and

breastfeeding practices.

Our findings indicate that observed child mortality declined from 105 to 77 per 1,000 live births between the first and last surveys, and most key health interventions now have greater coverage (Figure 2). Continued breastfeeding (beyond 6 months) was the only health intervention for which there was a decline in coverage. Substantial increases in coverage were found for bed net ownership, vaccination, access to family planning, antenatal care, intermittent preventive treatment for malaria during pregnancy, and prevention of mother-to-child transmission of HIV. The increases in coverage were relatively modest for maternal education, water, and sanitation.

Figure 2. Levels in mortality and intervention coverage between the first and last surveys (Source: DHS, https://dhsprogram.com/)

We found that urbanization, access to electricity, and maternal education appeared to have protective effects on child mortality. Only two of the seventeen public health interventions considered — continued breastfeeding and full vaccination coverage — appeared to be associated with reducing child mortality after controlling for socioeconomic factors. The impact of each intervention on child mortality was greatly heterogeneous within and across countries.

It may not come as a great surprise that vaccinations and breastfeeding duration made substantial contributions to reducing child mortality, and the same is true for education and general economic development. More surprising is that we did not find an effect for some interventions for which coverage has changed dramatically and which have been shown to have strong effects on child survival. This may be most striking for bed nets, where coverage has increased tremendously in recent years. One possible reason why bed net coverage was not shown to be effective in our analysis is that coverage increased more uniformly within countries (e.g. via mass distribution campaigns) compared with other interventions requiring greater health service infrastructure. If so, our study design, which relied on within-country variation over time, would not detect any positive effect of bed nets due to the country and survey fixed effects. It is also possible that reported bed net ownership is a poor indicator of whether children consistently sleep under the nets.

Overall, our findings likely underestimate the true impact that recent global health efforts have had on child survival. But even taking the numbers at face value, the overall effectiveness of those efforts can hardly be questioned. The current estimate of child mortality for sub-Saharan Africa is about three million deaths per year. More than six million children would likely die if the under-5 mortality rate had not changed since 1990. Of those extra three million child deaths we would have seen per year, we can directly attribute 50% of the improvement to key interventions at the regional level, thus corresponding to about 1.5 million child deaths prevented per year.

Development assistance for health has been growing, with donors disbursing $36.4 billion to improve health in low- and middle-income countries in 2015, a five-fold increase from 1990. Our findings suggest that expanded coverage of public health interventions has made substantial contributions to the mortality declines seen in sub-Saharan Africa over the past 25 years. While all socioeconomic variables considered appear to strongly predict health outcomes, this was true for very few health coverage indicators. These weak results may reflect a certain amount of measurement error but could also be interpreted as evidence of limited effectiveness of some interventions at scale. Further research should aim to more closely identify whether sufficient investments have been made to support effective interventions and why specific interventions may or may not work in certain settings.

Yoko Akachi is a global health consultant based in Helsinki, Finland. She currently works on reproductive health program impact evaluation and social health protection.

Maria Steenland is a doctoral candidate at Harvard T. H. Chan School of Public Health in the Department of Global Health and Population. She studies the effectiveness of interventions to improve health care coverage and quality.

Günther Fink is Associate Professor at the University of Basel and Head of the Household Economics and Health Systems Research Unit at the Swiss Tropical and Public Health Institute in Basel, Switzerland.

Health inequalities are on the rise in the United States: the gap in life expectancy between those at the top and the bottom of the income spectrum has increased rapidly since the dawn of the century, to the point where the lives of the poor are cut short by up to a decade and a half compared with those of the wealthy. Moreover, while the rich tend to live longer everywhere, life expectancy among the poor varies significantly by geographical region.

In our article recently published in the IJE, we show that these patterns of health are the product of powerful political and economic forces. Over the past few decades, neoliberal politics, the decline of unions and economic globalisation have resulted in rapid industrial restructuring and economic dislocation in the US. Organised labour has been eroded in the industrial heartland, and manufacturing operations have been shifted to the non-unionised south and to foreign countries.

Partially in response to the turbulence wrought by deindustrialisation, the penal system, rather than the welfare state, has served as a principal mechanism of regulating the increasingly marginalised working class. Since the mid 1970s, American jail and prison incarceration rates have reached a peak of almost eight inmates per 1000 residents, with an absolute number of more than 2.2 million people behind bars, which amounts to a sevenfold increase in four decades. Populations in areas of concentrated disadvantage that have undergone rapid economic decline have been shown to experience incarceration rates more than forty times higher than privileged White communities and three times higher than communities with similar crime rates. Most notably, for working-age African American men without a high school diploma, the life-course risk of imprisonment exceeds 60%.

Our analyses show that these macro-level developments in American society have potentially devastating consequences for population health: they disproportionately affect the poor and thus actively contribute to the deepening of health inequalities. Job destruction and prison incarceration rates at the state level are significantly associated with declines in the life expectancy of those in America’s lowest income quartile and could indeed account for much (if not the entire) increase in the health gap between the rich and the poor since 2001.

Our findings are relevant to major debates about inequality in the 21st century. They show that economic globalisation and deindustrialisation generate consequential health disadvantages among society’s most vulnerable. Current approaches to industrial policy must therefore be redefined if the threat of a widening health gap is to be taken seriously. Our findings also indicate that an appropriate political response to the ravages of economic decline would be to create social safety nets for working-class communities, rather than rolling out a penal apparatus which, in its current modus operandi, effectively does little but criminalise poverty.

Read more:

Nosrati E, Ash M, Marmot M, McKee M, King LP. The association between income and life expectancy revisited: deindustrialization, incarceration and the widening health gap. International Journal of Epidemiology, dyx243, https://doi.org/10.1093/ije/dyx243.

Elias Nosrati is a Cambridge Trust International Scholar at the University of Cambridge. His research focuses on the political economy of public health and the interface between social and medical sciences.

Michael Ash (@michaelaoash) is Professor of Economics at the University of Massachusetts, Amherst. His research focuses on labour economics, environmental change and health disparities.

Sir Michael Marmot (@MichaelMarmot) is Professor of Epidemiology and Public Health and Director of the Institute of Health Equity at University College London, where he studies the social determinants of health.

Martin McKee (@martinmckee) is Professor of European Public Health at the London School of Hygiene and Tropical Medicine. His main research foci are health determinants, health system performance and the relationship between health and the economy.

Lawrence P King is Professor of Economics at the University of Massachusetts, Amherst. His work focuses on the comparative study of socioeconomic transitions and the political economy of public health.

Traditionally, asthma and type 1 diabetes have been considered distinct immune-mediated diseases in which the underlying immune responses counteract each other, resulting in an inverse association between the diseases. In our study, recently published in the IJE, we explored the association between asthma and type 1 diabetes in childhood in a novel way, and observed that the direction of the association is dependent on the order of appearance of the diseases.

Increasing numbers of children and adolescents have diseases that are linked to inappropriate function of the immune system, such as asthma, allergic diseases and type 1 diabetes. However, the reasons for the parallel increases in incidence, or how the diseases are related, constitute an unsolved puzzle. Inconsistencies in the findings of previous observational studies and increasing evidence of the complexity of the immune responses related to both asthma and type 1 diabetes have brought into question the traditional view of an inverse association.

We used large, nationwide Finnish health registers to obtain information on asthma and type 1 diabetes diagnoses up to the year 2009 for all children born between 1981 and 2008. Our case-cohort study included 9541 children with type 1 diabetes, 81,473 with asthma and a reference cohort of 171,138 children. From the health registers, we also obtained information on various maternal and child background characteristics. To allow the sequential order of the diseases and the age of diagnosis to vary, we used a multistate modelling approach in our statistical analysis.

Our main finding was that the association between these diseases depended on the order of their appearance: if asthma had been diagnosed first, children had an increased risk of developing subsequent type 1 diabetes, compared with children who developed only type 1 diabetes. On the other hand, children who already had type 1 diabetes had a decreased risk of developing subsequent asthma, compared with children who developed only asthma. This curious phenomenon was seen in all age groups studied, and the results held true even after taking into consideration the sex and birth decade of the child, maternal asthma or diabetes and various other sociodemographic and perinatal factors.

What could explain why having asthma increases the risk of type 1 diabetes, but not the other way around? Our suggestion that use of inhaled corticosteroids may play a role in the development of type 1 diabetes is biologically plausible, although a novel hypothesis. However, the lack of potentially important information in our register data needs to be considered. For example, we did not have information on early dietary factors and infections, both of which have been linked to the development of asthma and type 1 diabetes. The original immunological explanation for an inverse association may be applicable to our observation that less asthma occurred after the development of type 1 diabetes.

It would be interesting to see if similar associations occur in other paediatric populations or with other allergic and autoimmune diseases. It is worth noting that Finland has the highest incidence of childhood type 1 diabetes in the world, while the prevalence of asthma is lower than in countries such as the UK and Australia, which have a high prevalence of asthma. It would also be interesting to see whether pre-existing asthma is an important confounder or effect modifier for the association between different environmental factors and the development of type 1 diabetes.

Our results support the view that an inverse association between asthma and type 1 diabetes is likely an oversimplification and that the association is more complex than previously thought. Sensitivity analyses using conventional analysis methods further strengthen our conclusion that the sequential order and timing of the diseases are important considerations for obtaining valid estimates of the association.

Although our study provided interesting new findings on the association between asthma and type 1 diabetes, no firm explanations or clinical implications can yet be drawn. However, our results further highlight the need for a wider perspective when exploring the causes of childhood immune-mediated diseases. The evidence is growing that asthma and type 1 diabetes may have common features (i.e. shared risk or protective environmental and genetic factors) in their development, but the causes of these diseases have traditionally been investigated by distinct research groups. There is thus a global need for interdisciplinary activities to better understand the complex relationships between, and determinants of, the broad range of childhood immune-mediated diseases.

Johanna Metsälä (PhD) is a Visiting Researcher at the National Institute for Health and Welfare, Finland. Her research is focused on early-life environmental factors and the development of asthma, allergic diseases and type 1 diabetes, with a special emphasis on using register-based data.

Jaakko Nevalainen is a Professor of Biostatistics in the University of Tampere, Finland. His collaborative research is focused on modelling in longitudinal studies on type 1 diabetes, prostate cancer and nutrition, and his theoretical research is mainly on the framework of clustered, multivariate data and with potentially informative cluster size.

Suvi M Virtanen is a Research Professor and Head of Nutrition Unit at the National Institute for Health and Welfare, Finland, and a Professor of Epidemiology in the University of Tampere. Her research is focused on maternal and child nutrition and growth in the development of type 1 diabetes, asthma, allergic diseases, overweight and obesity in childhood. Twitter: @suvi_m_virtanen

]]>https://ije-blog.com/2017/12/04/asthma-and-type-1-diabetes-in-childhood-new-insights-into-their-association/feed/0ijeeditorialMetsaela_authorsHaving more frequent social contact is associated with better cognitive performancehttps://ije-blog.com/2017/11/09/having-more-frequent-social-contact-is-associated-with-better-cognitive-performance/
https://ije-blog.com/2017/11/09/having-more-frequent-social-contact-is-associated-with-better-cognitive-performance/#respondThu, 09 Nov 2017 04:03:32 +0000http://ije-blog.com/?p=1991Continue reading Having more frequent social contact is associated with better cognitive performance]]>Andrew Sommerlad and Marko Elovainio

Dementia is the most feared aspect of ageing and is a major global health challenge, so identifying lifestyle factors that can reduce memory decline, and possibly prevent dementia from occurring, is a research priority. In our study, recently published in the IJE, we explored whether having more frequent contact with friends and family, or being married, is linked to better memory and language in older age.

We found that having more social contact and being married in mid-life were both linked to having better cognitive performance over the next 20 years. In particular, we found that verbal fluency was the cognitive area with the strongest link to social contact.

Our study cannot tell us the direction of the relationship — whether social contact is the cause of better cognitive performance, or its effect. To do this, we would need to test whether active measures to increase people’s social contact in their middle-aged years strengthen cognition in later life. Considering that nearly three-quarters of older people report feeling lonely, taking such measures may make a difference to their quality of life as well as their cognition.

For our study, we used the Whitehall II cohort of 10,000 London-based civil servants (including manual and clerical staff and those from higher professional grades) who were first interviewed in the mid 1980s and continue to have their physical, mental and cognitive health assessed at 5-yearly intervals. Whitehall is one of the UK-based research studies that were originally set up to examine influences on general physical health, and it is now being used to examine the priority research areas of cognition and dementia risk.

We used data from Whitehall interviews between 1985 and 1990 in which participants were asked:

how often they saw family and friends and how often they participated in social and religious activities (scored on a 28-point scale), and

whether they were married — we saw this as another way of measuring social contact, as other studies have suggested that being married leads to more lifetime social contact.

To assess cognition, we used three different tests, measured on five occasions over the subsequent 20 years. To assess memory, we showed participants 20 words and asked them to recall as many as possible 2 minutes later. For verbal fluency, we asked people to think of as many animals and then as many words beginning with “s” as possible in 1 minute. Finally, to assess verbal and mathematical reasoning, we used a timed test in which we asked a series of increasingly difficult reasoning questions.

From the results of these tests, we identified three distinct subgroups of study participants who had similar patterns of cognitive change throughout the study period, which we classified as high, intermediate or low cognitive performance. The graph below shows the average cognitive change in the three groups across the 20 years. From the initial average performance results, there was a slight increase in performance at the second test for the high and intermediate cognitive performance groups, which we believe was because the participants were more familiar with the test on the second sitting (the “practice effect”). All groups then had a gradual decline in cognitive performance over the next 15 years.

We then analysed whether people’s previous social contacts influenced their cognitive trajectory and found that each extra point scored on the social contact scale (such as seeing family weekly rather than monthly) was linked to a 4% lower chance of being in the low cognitive performance group. People who were married had a 30% lower risk than those who were unmarried. These findings held true even when we took into account a range of other health and lifestyle factors, such as age, sex, ethnicity, weight and alcohol consumption.

Although other research studies have previously found a link between infrequent social contact and lower cognitive ability, our study had the advantage of using data with a long follow-up and multiple measurements of cognition, which helped us to better understand the long-term outcomes. As well as testing whether these results hold true in other populations, a potential next step is to test whether improving social contact can have benefits for cognition. However, finding effective ways to do this that would be acceptable to the most socially isolated groups, many of whom may be reluctant to make changes, is a major challenge. Overcoming this challenge could have substantial benefits for individuals and society.

Andrew Sommerlad is a Wellcome Trust Research Fellow at the UCL Division of Psychiatry and an old-age psychiatrist at Camden and Islington NHS Foundation Trust. His research focuses on social engagement and dementia, including whether social contact protects against the disorder, and the effect of social isolation on the likelihood of receiving a dementia diagnosis. (Twitter: @atsommerlad)

Marko Elovainio has tenure as a professor of psychology at the University of Helsinki and part-time tenure as a research professor at the Finnish National Institute for Health and Welfare. His research has focused on social epidemiology, intergenerational transmission of health, occupational health psychology and the risk factors for depression, cardiovascular diseases and type 2 diabetes.

Rising mortality among young and middle-aged White Americans has alarmed researchers, public health professionals and the broader public. These concerns were amplified by a 2015 study in which the authors attributed rising mortality rates among White Americans to increases in deaths from chronic liver disease, suicide and drug overdoses. The authors argued that increased mortality from these causes of death is likely a result of the “same underlying epidemic” that is affecting a “lost generation” of Americans. The underlying epidemic was said to be “deaths of despair”, originating from rising distress, economic insecurity and chronic pain.

Media outlets covered this narrative extensively, with several commenting on the struggles and decline of White America that enabled this trend in rising mortality. The 2016 Presidential election also brought speculation that the success of Donald Trump was due in part to the social breakdown and economic challenges afflicting poor, rural, White Americans.

The evidence supporting deaths of despair, however, is quite weak. The study that pushed this narrative was met with scepticism about its methods and interpretation, with some arguing that the findings were misleading due to “age-aggregation bias”. It was correctly pointed out that between 1999 and 2013, the average age of people in the 45–54-years age group increased considerably. With more people in this age group being in their 50s, the mortality rate might naturally increase, as mortality is more common at older ages. In fact, adjusting for the age composition of the population could account for a large percentage of the reported mortality increases.

In our study recently published in the IJE, we find little empirical support for the pain- and distress-based narratives. We show that mortality increases have likely been shaped by the US opiate epidemic and stalled progress in reducing deaths related to metabolic diseases. While we do not question the severe public health consequences of economic insecurity or the harsh realities of chronic pain and addiction, existing research and media reports have advanced a narrative that is simply not supported by the data.

The foundation of the deaths of despair explanation was a study that analysed a small age group (45–54 years), during a select period of time (1999–2013), while combining deaths from separate causes for men and women. In our study, we analysed women and men separately for cause-specific mortality from suicides, alcohol poisonings, drug poisonings, metabolic diseases and causes external to the body (such as complications from childbirth or pregnancy, nutritional deficiencies and accidents other than drug or alcohol poisonings). Further, we extended the analysis to mortality rates between 1980 and 2014, for both younger (25–34 years) and middle-aged (35–54 years) White Americans.

We grouped our findings into four main points, each of which are relevant to mortality research and public health policy. First, there are considerable gender differences in White American mortality trends, which are reflected in all-cause mortality rates and cause-specific trends. Notably, to some extent, the gender differences in mortality from external causes of death reflect HIV/AIDS-related deaths that plagued middle-aged men in the 1990s but which continued to shape White men’s mortality well into the 2000s. Additionally, while men and women both experienced increased drug-related mortality, there are differences in the onset, level and ages most affected. We would expect to find similar trends for men and women if the increases in White mortality had been driven by the “same underlying epidemic”.

Second, and most importantly, we found that mortality trends are not consistent for the despair-related causes. For example, we found that the relative contribution to overall mortality from drug-related deaths increased dramatically in the 1990s and continued through the 2010s, but we observed no sizeable increases in suicide or alcohol-related deaths for White men or women. This would imply that the underlying causes driving these mortality trends are likely different.

Third, rising drug-related mortality does not reflect rising mortality among a “lost generation” of White Americans, as increases in drug-related deaths were not confined to mid-life ages. Given that we found that all ages (25–54 years) experienced similar rapid increases in drug-related mortality, we find this inconsistent with a narrative of increasing pain and despair plaguing a single generation. Instead, the timing of the increases coincides with the rising availability, over-prescription and misuse of opioid-based painkillers, such as oxycodone, which increased addiction and heroin use.

Fourth, successes in reducing mortality from metabolic diseases (i.e., heart disease, obesity, hypertension) have slowed among White men and stalled among White women. This important point is missed in the despair narrative, as overall mortality rates would likely not have increased for middle-aged Americans without this slowed progress. Further, while drug-related mortality increases reflect a period-based phenomenon affecting multiple generations of Americans, we found evidence to suggest that mortality risk from metabolic disease is rising substantially across cohorts and affecting younger Americans more strongly than previous generations. These results likely represent the onset of health consequences related to the US obesity epidemic.

To conclude, our findings do not support the deaths of despair narrative, which argues that a generation of middle-aged White Americans is suffering from an underlying epidemic of distress, uncertainty and pain. If this were the case, we would expect to observe similar increases in mortality from all three causes for both men and women. Our findings illustrate that mortality increases for White Americans have largely been driven by period-based increases in drug poisoning deaths and cohort-based increases in metabolic disease deaths, related to the US opioid epidemic and the US obesity epidemic, respectively.

Daniel Simon is a PhD student in the Department of Sociology at the University of Colorado Boulder and is affiliated with the CU Population Center at the Institute of Behavioral Science. His research focuses on population–environment interactions in Mexico and recent trends in US mortality and is funded by the National Science Foundation through a Graduate Research Fellowship award (Twitter: @SimonSOCY).

Andrea Tilstra is a PhD student in the Department of Sociology at the University of Colorado Boulder and a graduate research assistant for the CU Population Center at the Institute of Behavioral Science. Her research interests are primarily in the areas of social demography and population health, and she is particularly interested in how US mortality and fertility vary across time and space, and how these variations align with changes in public policy (Twitter: @Andrea_Tilstra).

Ryan Masters is an assistant professor of sociology and a faculty associate in the Population Program and Health & Society Program in the Institute of Behavioral Science at the University of Colorado Boulder. His work examines social differences in US health and mortality trends.

Only a few years ago, doctors would advise their patients that elevated blood levels of high-density lipoprotein cholesterol (HDL-C), then termed the “good cholesterol”, were beneficial and would protect them against coronary heart disease. This belief has been called into question, however, as neither genetics nor clinical trials could demonstrate that raising HDL-C levels would protect against cardiovascular disease. Our study, published recently in the IJE, casts further doubt on this “not-so-good-anymore” cholesterol by showing that genetic variants that cause higher HDL-C levels also increase the risk for age-related macular degeneration (AMD).

AMD is the leading cause of vision loss in the elderly worldwide, and in the United States it affects more than twice as many people as Alzheimer’s disease. A long line of epidemiological studies indicated a relationship between HDL-C and AMD. However, results of these studies have been inconsistent, and researchers could concur neither on a directionality of effects nor whether the assumed relationship was direct or indirect.

More recently, research into human genetics has shed further light on this issue by discovering, through genome-wide association studies (GWAS), that genetic variants in a few genes that raise HDL-C levels also elevate AMD risk. For instance, through GWAS in Europeans, a common allele (rs3764261) near the lipid-regulating gene CETP was found to be associated not only with higher plasma HDL-C levels, but also with AMD risk (odds ratio, 1.15). This was further supported by findings from East Asians that a coding variant in CETP (D442G) that increases plasma HDL-C levels also strongly increased the risk of exudative AMD (per allele odds ratio, 1.7).

Our study further solidifies the link between HDL-C and AMD by demonstrating that, in general, common polymorphisms that modify plasma HDL-C levels also have an impact on AMD risk, and that genetically increased levels of HDL-C increase the risk of AMD.

We chose to test 185 common genetic variants associated through GWAS with plasma lipid levels that had independently also been analysed for their impact on AMD risk. We then applied Mendelian randomisation, a method that leverages the random allocation of DNA variants at birth to test for a causal relationship between a modifiable risk factor (HDL-C) and a disease outcome (AMD risk). The association between HDL-C and AMD remained robust using three alternative Mendelian randomisation models, while variants that modify other lipid species fractions in the blood, particularly “bad” low-density lipoprotein cholesterol and triglyceride levels, did not co-associate with AMD risk.

These observations are consistent with a recent similar study involving people of predominantly European descent. Importantly, our results agree with and extend on this work through direct analysis of the full European-ancestry summary statistics and replication in an independent sample of East Asian ancestry. In total, our results are based on a sample of more than 40 000 people with European and East Asian ancestry, establishing that the link between HDL-C and AMD risk is generalisable beyond a single ethnicity.

Our study thus proposes HDL-C as a potentially key risk factor during AMD pathogenesis. However, this comes with several unknowns. First, the mechanisms that link HDL-C and AMD remain entirely unclear. For instance, we do not yet know whether the culprit for the association is in the blood or whether yet unknown lipid-regulatory mechanisms specific to the eye may play a role. Second, we observed considerable differences in the extent by which HDL-C variants affect AMD risk across populations, loci and subtypes of AMD — the reasons for this remain unexplained. Finally, there are limitations in the Mendelian randomisation approach used in our study. Specifically, we do not yet know how well the insights gained from evaluating the effect of genetic (i.e. lifelong) exposure to elevated HDL-C levels on AMD risk translate into changes to HDL-C levels during one’s lifetime through environmental exposures. Furthermore, our study was designed to assess effects of HDL-C on risk of developing disease, rather than effects on disease activity in people who already have or are in the process of developing AMD.

The latter point will be particularly important for assessing whether drugs that reduce HDL-C levels could be of benefit to treat or prevent AMD. Of potentially more importance is that drugs that elevate HDL-C levels — ranging from statins that mildly increase HDL-C, to niacin that elevates HDL-C by more than 20% — are routinely being used in the treatment of cardiovascular disease. It can thus be expected that all “eyes” will be on a new generation of drugs that target CETP to elevate HDL-C levels and reduce cardiovascular events. The results of a large Phase III cardiovascular outcome trial in about 30 000 patients for one of these drugs, anacetrapib, have recently been released.

It will be interesting to see clinical data emerge that could help to further assess putative risks caused by HDL-C-raising therapies, as well as to validate the suitability of Mendelian randomisation to assist therapy development.

Joe Maranville is an associate principal scientist at Merck Research Labs in Boston in the USA. He has a background in human genetics (PhD) and clinical pharmacology (certified by American Board of Clinical Pharmacology). His work focuses on the application of statistical genetics to inform drug development, especially integrative analyses of intermediate traits and clinical outcomes.

QiaoFan is a senior research fellow at the Centre for Quantitative Medicine, Duke-NUS Medical School, in Singapore. Her research focuses on gene mapping, gene–environment interactions, causal inference, risk prediction modelling using high-dimensional data, and genomics of common eye diseases.

Ching-Yu Cheng is an associate professor at Duke-NUS Medical School and principal clinician scientist at Singapore Eye Research Institute. His work involves a variety of epidemiological and clinical research into age-related ocular diseases, as well as identification of susceptibility genes for complex ocular phenotypes, using both genome-wide association approaches and next-generation sequencing.

Tien Wong is professor and medical director of Singapore National Eye Center, Duke-NUS Medical School, National University of Singapore. He is a retinal specialist and leads a broad-based research program comprising epidemiological, clinical and translational studies of retinal diseases, such as diabetic retinopathy and age-related macular degeneration.

HeikoRunzis the head of translational genetics at Merck Research Labs in Boston. He is a board-certified medical geneticist and translational scientist with a track record in clinical, Mendelian and complex genetics.His current research spans from translating genetic discoveries into function to informing clinical drug development programs on medical and business needs.